Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dementia is going to be one of the major challenges of the next century for our societies due to the enormous burden on the health care systems. Dementia is the major cause of death and the most important risk factor for disability and entry into a nursing home in elderly people. Moreover, because of the progress in the treatment of Alzheimer's disease, in particular with the cholinesterase inhibitors, demented people will be more often and detected earlier by general practitioners and families. Thus, dementia will become progressively more a public problem than a private one. This tendency could be increased by the unemployment problem among young adults which obliges their parents to support them, neglecting then their own parents' problems. A possible way to win this challenge is prevention. Intervention on several risk factors of dementia in the elderly is possible. The Syst-Eur trial demonstrated recently that treatment of systolic high blood pressure could decrease the risk of dementia by 50%. Other vascular risk factors, depression, aluminium in drinking water, and active life are other good candidates for preventive intervention. Finally, secondary prevention by treatment among people with mild cognitive impairment will be another interesting way of delaying the onset of the disease and decrease it's prevalence.
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PMID:Dementia: epidemiology, intervention and concept of care. 1065 78

Factors accelerating cerebral degenerative changes represent potentially modifiable risks for cognitive decline. Putative risk factors accelerating mild cognitive decline and dementia were correlated with repeated measures of cerebral atrophy, CT densitometry, perfusions and cognitive testing among neurologically and cognitively normative volunteers. TIAs, hypertension, smoking and male gender accelerate cerebral degenerative changes, mild cognitive decline and dementia. Intervention by control of risk factors and cholinesterase inhibitors should prevent cerebral atropho-degenerative changes so that optimal cognitive performance is maintained.
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PMID:XE-CT CBF changes during normative aging, cognitive decline and dementia. 1075 Mar 50

Many women with cerebrospinal fluid shunts are now reaching reproductive age. Clinical management of pregnant patients with hydrocephalus should include preconception counseling and CT scan or MRI. A family pedigree should also be established for counseling on the risk of recurrence of the woman's condition or another neural tube defect. Electrophoresis of acetylcholinesterase in the amniotic fluid can provide the diagnosis of open neural tube defect between 13 and 24 weeks gestation. Shunt malfunction may occur during pregnancy in 50 % of cases. Management requires well-planned, a combined neurosurgical and obstetrical approach. Vaginal delivery is possible in asymptomatic mothers. Cesarean section is recommended for neurologically unstable patients. Prophylactic antibiotics are recommended for labor and delivery to avoid shunt infection. Epidural analgesia is contraindicated in patients with intracranial hypertension. Some complications of complementary treatment for cerebral tumors in childhood are briefly reported.
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PMID:[Hydrocephalus during pregnancy with or without neurosurgical history in childhood. Practical advice for management]. 1084 53

We investigated the cardiovascular consequences of acute intoxication by the organophosphate poison, mevinphos (Mev), and delineated the underlying mechanism. Based on on-line power spectral analysis of systemic arterial pressure (SAP) signals in rats anesthetized and maintained by propofol, we identified two distinct phases after intravenous administration of Mev (160 or 320 microg/kg). Phase I was characterized by transient hypertension and mild tachycardia, concurrent with an increase in the very high-frequency (BVHF; 5-9 Hz), high-frequency (BHF; 0.8-2.4 Hz), low-frequency (BLF; 0.25-0.8 Hz),and very low-frequency (BVLF; 0-0.25 Hz) components of SAP signals. Phase II exhibited significant hypotension, a reversal of the BVHF and BVLF power to control levels, and further reduction in the power density of both BHF and BLF components to below baseline. Microinjection of Mev (2 microg) into the bilateral nucleus reticularis ventrolateralis (NRVL), the medullary origin of sympathetic neurogenic vasomotor tone, essentially duplicated those phasic cardiovascular changes. Similarly, sympathoexcitatory NRVL neurons exhibited respectively an elevation and a decline in their spontaneous activities during Phase I and Phase II Mev intoxication. We conclude that the progressive accumulation of acetylcholine over time induced by a direct inhibition of Mev on cholinesterase in the NRVL may be responsible for the phasic changes in cardiovascular events over the course of acute Mev intoxication. Whereas the initial amount of acetylcholine is excitatory to NRVL neurons, overstimulation by the amassed acetylcholine results instead of an inhibitory action.
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PMID:Spectral changes in systemic arterial pressure signals during acute mevinphos intoxication in the rat. 1119 55

Our laboratory has found that the organophosphate pesticide chlorpyrifos elicits an elevation in blood pressure that persists for approximately 24 hr after exposure. Since organophosphate pesticides inhibit acetylcholinesterase activity and cause cholinergic stimulation in the central nervous system and peripheral tissues, we suspect that the hypertensive response from chlorpyrifos is elicited by activation of pressor areas in the brain stem, specifically muscarinic receptors which are known to mediate hypertensive responses. Oxotremorine, a muscarinic agonist, should elicit a blood pressure response similar to organophosphate pesticides. This study used radiotelemetry to assess the effects of oxotremorine on blood pressure, heart rate, core temperature, QA interval (a measure of cardiac contractility), and motor activity in the male, Long-Evans rat. Subcutaneous co-administration of 0.2 mg/kg oxotremorine with 1.0 mg/kg methyl scopolamine (i.e., to block oxotremorine's peripheral effects) caused a marked elevation in blood pressure that developed concomitantly with a 2 degrees decrease in core temperature, 60 beats/min. increase in heart rate, increase in cardiac contractility but no change in motor activity. Overall, blood pressure increased by 19 mmHg from baseline and the response persisted for approximately 12 hr after injection. Methyl scopolamine alone increased heart rate but had no effect on blood pressure, core temperature, and motor activity. Oxotremorine injected without methyl scopolamine led to a relatively minor increase in blood pressure and hypothermia. Overall, central muscarinic stimulation with oxotremorine and methyl scopolamine leads to a vigorous hypertensive response that is associated with increased cardiac contractility, suggesting an increase in cardiac output. Combined central and peripheral cholinergic stimulation following oxotremorine without methyl scopolamine, as would also occur with exposure to chlorpyrifos and other organophosphate pesticides, did not elicit as much of a hypertensive response. This would suggest pathways other than those controlled directly with muscarinic receptors are operative in the development of chlorpyrifos-induced hypertension.
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PMID:Peripheral versus central muscarinic effects on blood pressure, cardiac contractility, heart rate, and body temperature in the rat monitored by radiotelemetry. 1148 8

The past decade has seen a renewed interest in vascular dementia. The search for a causal relationship between a vascular event or a vascular cerebral lesion and dementia has led to new classification schemes which no longer consider vascular dementia a homogeneous entity but acknowledge the diversity of the clinical and morphological substrates of this syndrome. Deviation from the term "multi-infarct dementia" is only one but many consequencies of these recent developments. Etiologically, vascular dementia may result from cerebral small vessel disease leading to extensive leucencephalopathy or lacunes or may be the consequence of strategically located infarcts or multiple infarcts in large vessel territories. It may also be the consequence of global cerebral hypoperfusion, intracerebral hemorrhage or other mechanisms such as vasculitis. There is no definitive medical or surgical treatment for vascular dementia. Thus, it appears that stroke prevention offers the most immediate and substantial solution to reduce the morbidity and mortality. This is best substantiated for treatment of arterial hypertension. Once vascular dementia occurs control of vascular risk factors may be useful but this contention will require larger scale studies to provide more definite proof. A number of metabolically active drugs has been used for the treatment of cognitive symptoms in vascular dementia. Yet, the data are conflicting und the effects described modest at most. There is epidemiological evidence for a more than incidental co-existence between vascular and primary degenerative dementia which suggests that therapies found to be effective in Alzheimer's disease may also prove beneficial at least in subgroups of vascular dementia. Lately, this concept is tested by several studies on the efficacy of acetylcholinesterase inhibitors in vascular dementia.
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PMID:[Vascular dementia]. 1192 78

We have previously reported that the angiotensin system in the anterior hypothalamic area (AHA) is enhanced in spontaneously hypertensive rats (SHR) and that this enhancement is involved in hypertension in SHR. In addition, acetylcholine (ACh) release is increased in the rostral ventrolateral medulla (RVLM) of SHR, which has also been shown to be involved in hypertension in SHR. In this study, we examined whether the enhanced angiotensin system in the AHA of SHR is related to the increase in cholinergic inputs to the RVLM. Electrical stimulation in the AHA produced a pressor response and an increase in firing rate of RVLM barosensitive neurons. These responses were inhibited and enhanced by RVLM application of the muscarinic receptor antagonist scopolamine and the cholinesterase inhibitor physostigmine, respectively. AHA stimulation also produced release of ACh in the RVLM. Microinjections of angiotensin II and carbachol into the AHA produced pressor responses. The pressor response to angiotensin II was inhibited by scopolamine microinjected into the RVLM, although this produced no effect on the response to carbachol. In SHR, although not in Wistar-Kyoto rats, microinjection of losartan into the AHA inhibited pressor responses to physostigmine. However inhibition was not observed in response to the directly acting muscarinic receptor agonist carbachol, injected into the RVLM. These findings demonstrate that angiotensin receptor activation or electrical stimulation in the AHA produce a pressor response via an increase in ACh release in the RVLM. In addition, the present study suggests that the enhanced angiotensin system in the AHA of SHR increases cholinergic inputs to the RVLM, which leads to increases in blood pressure.
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PMID:Activation of hypothalamic angiotensin receptors produces pressor responses via cholinergic inputs to the rostral ventrolateral medulla in normotensive and hypertensive rats. 1238 57

Between 20 and 35% of all dementias are vascular in origin, their etiology is due to cerebrovascular disease and the risk factors are known (e.g. hypertension, diabetes, smoking, or hyperlipidemia). Primary and secondary preventions are the basis of therapeutics. Symptomatic treatment is emerging, notably in the field of cognitive disorders. In that respect, monoamine oxidase inhibitors, and more recently acetylcholinesterase inhibitors, are in the process of being recognized as first-line treatments of established vascular dementia.
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PMID:Drugs and vascular dementia. 1271 93

Vascular dementia (VaD) is the second-most-common cause of dementia in the elderly, after Alzheimer's disease (AD). VaD is defined as loss of cognitive function resulting from ischemic, hypoperfusive, or hemorrhagic brain lesions due to cerebrovascular disease or cardiovascular pathology. Diagnosis requires the following criteria: cognitive loss, often predominantly subcortical; vascular brain lesions demonstrated by imaging; a temporal link between stroke and dementia; and exclusion of other causes of dementia. Poststroke VaD may be caused by large-vessel disease with multiple strokes (multiinfarct dementia) or by a single stroke (strategic stroke VaD). A common form is subcortical ischemic VaD caused by small-vessel occlusions with multiple lacunas and by hypoperfusive lesions resulting from stenosis of medullary arterioles, as in Binswanger's disease. Unlike with AD, in VaD, executive dysfunction is commonly seen, but memory impairment is mild or may not even be present. The cholinesterase inhibitors used for AD are also useful in VaD. Prevention strategies should focus on reduction of stroke and cardiovascular disease, with attention to control of risk factors such as hypertension, diabetes mellitus, hypercholesterolemia, and hyperhomocysteinemia.
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PMID:Vascular dementia: distinguishing characteristics, treatment, and prevention. 1280 86

A cure for Alzheimer's disease (AD) is still far off, and clinicians face the burden of caring for patients at all stages of dementia for the foreseeable future. Those with advanced disease suffer neurological symptoms and signs that include incontinence; problems with gait and mobility; marked cognitive, language, and functional impairment; and in about 90% of patients, significant behavior problems. Dementia precludes the ability to initiate meaningful activities or social interactions. Whether patients are resident in the community or living in a nursing home, this composite reflects a highly complex medical and neuropsychiatric management challenge. Predictable medical conditions also must be addressed (i.e., those that accompany dementia, such as parkinsonism, and those that are prevalent in any aging population, such as hypertension). Clinicians can better address these problems with awareness of current treatment options. Placebo-controlled trials of some psychotropic agents have shown modest favorable effects on behavior problems. Use of acetylcholinesterase inhibitors (AChEIs) to treat cognitive impairment and secondary behavioral symptoms derives primarily from results of placebo-controlled clinical trials. Trials in patients with moderate to severe AD, outpatients as well as nursing home residents, show overall effects similar to those seen in outpatients with milder dementia. Treatment with AChEIs may delay institutional placement. Memantine has shown benefit in trials in moderate to severe dementia, although it is not yet approved in the United States. Emerging data have expanded physicians' ability to use pharmacotherapy in patients with advanced dementia. Physicians need to enact the principle that something can be done for our afflicted parents and grandparents.
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PMID:Medical management of advanced dementia. 1280 87


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